Intracranial hemorrhage (ICH) causes high mortality and disability without effective treatment in the clinical setting. (−)-Epigallocatechin-3-gallate (EGCG) exerts an essential role in the central nervous system and offers a promising therapeutic agent for the treatment of oxidative damage-related diseases. MiR-137 can inhibit the oxidative stress and apoptosis to attenuate neuronal injury. However, the role of EGCG in regulating miR-137-3p and neuronal Parthanatos remains to be unclear. In the present study, we build the ICH mice model to investigate the antioxidant effects of EGCG via upregulating miR-137-3p and inhibiting neuronal Parthanatos. We revealed that EGCG upregulated miR-137-3p and inhibited neuronal Parthanatos, and promoted the functional recovery, alleviated ICH-induced brain injury, and reduced oxidative stress in mice following ICH. However, following the inhibition of miR-137-3p and activation of Parthanatos, EGCG was unable to exert neuroprotective roles. These combined results suggest that EGCG may upregulate miR-137-3p and inhibit neuronal Parthanatos to accelerate functional recovery in mice after ICH, laying the foundation for EGCG to be a novel strategy for the treatment of neuronal injuries related to Parthanatos.

中文翻译：

---

EGCG通过上调miR-137-3p和抑制Parthanatos治疗ICH

颅内出血（ICH）在临床环境中没有有效的治疗方法会导致高死亡率和残疾。（-）-Epigallocatechin-3-gallate（EGCG）在中枢神经系统中发挥重要作用，并为治疗与氧化损伤相关的疾病提供了有希望的治疗剂。MiR-137可以抑制氧化应激和细胞凋亡，从而减轻神经元损伤。然而，EGCG在调节miR-137-3p和神经元Parthanatos中的作用尚不清楚。在本研究中，我们建立ICH小鼠模型，以通过上调miR-137-3p和抑制神经元Parthanatos来研究EGCG的抗氧化作用。我们发现EGCG上调了miR-137-3p并抑制了神经元Parthanatos，并促进了功能恢复，减轻了ICH引起的脑损伤，和降低ICH后小鼠的氧化应激。但是，在抑制miR-137-3p和激活Parthanatos之后，EGCG无法发挥神经保护作用。这些综合结果表明，EGCG可能会上调ICH后小鼠的miR-137-3p并抑制神经元Parthanatos从而加速功能恢复，这为EGCG成为治疗与Parthanatos相关的神经损伤的新策略奠定了基础。